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GI Physiology
| Question | Answer |
|---|---|
| Which digestive process predominates in carnivores, enzymatic or microbial? | Enzymatic |
| What is the difference between ruminants and horses with regard to the site of fermentation relative to the stomach? | Horses are postgastric fermenters, meaning that microbial digestion occurs after their acid-producing stomach. Cows are pregastric fermenters, meaning that microbial digestion occurs before the acid-producing stomach. |
| Why does a herbivorous diet require greater eating time than a carnivorous diet? | A herbivorous diet consists of low-energy meals, requiring more time to extract all available energy from food while a carnivorous diet consists of high-energy meals. |
| How does the ruminant maintain blood glucose concentration? | Ruminants produce glucose in the liver from the SCFA's to maintain blood glucose concentration. |
| What happens to the dietary protein digested by ruminants? | Dietary protein digested by ruminants is digested by microorganisms in the rumen. |
| How can NPN be utilized by ruminants? | NPN is utilized by microorganisms to produce microbial protein, which is digested in the small intestine. |
| What is the major end product of carbohydrate digestion in the horse? | Glucose |
| Why are horses less efficient than ruminants in digesting fiber? | Ruminants digest insoluble fiber more efficiently due to extended microbial digestion in the rumen. Horses have a shorter, postgastric fermentation process that extracts less energy from food. |
| Name the layers of the intestinal wall in their order of appearance from lumen to serosa. | -Mucosa (epithelium and lamina propria, muscularis mucosae) -Submucosa -Muscularis externa (circular muscle, longitudinal muscle) -Serosa |
| What two plexuses have ganglia located in the intestinal wall? What are their locations? | The submucosal plexus is located in the submucosa, and the myenteric plexus is located between the inner circular muscle layer and the longitudinal muscle layer. |
| What central components mediate neural control of gut function? | Neural control of gut function is mediated by ANS (para and sympathetic) and the ENS (myenteric and submucosal plexuses). |
| What are the receptors for preganglionic and postganglionic neurotransmitters? | Pre: Cholinergic receptors in sympathetic system; Nicotinic, cholinergic in parasympathetic Post: Adrenergic receptors as well as neuropeptide Y and/or somatostatin receptors in sympathetic system; muscarinic cholinergic in parasympathetic |
| Where do parasympathetic, preganglionic neurons synapse? What is the major transmitter at this location? | Parasympathetic, preganglionic neurons synapse in the submucosal and myenteric plexuses. The major transmitter at these plexuses is ACh. |
| Where are the muscarinic, cholinergic receptors located for the parasympathetic postganglionic neurons? | Receptors are located in the muscle or epithelium of the intestine. |
| Are the neuronal circuits of the ENS dependent on the CNS? | No. Basic peristaltic reflexes can occur without CNS input. |
| In general, what are the effects of the cholinergic and adrenergic innervation on contractile activity and secretion? | Cholinergic: increases contractile activity and secretion Adrenergic: inhibits motility, secretion, and blood flow |
| Name two ways in which adrenergic stimulation can exert its inhibitory effects. | Adrenergic stimulation inhibit ACh release from preganglionic or postganglionic cholinergic fibers, creating both direct and indirect inhibitory effects. |
| What are the effects on epithelium and smooth muscle of ENS motor neurons containing ACh? | Excitatory actions: in muscle, the longitudinal muscle contracts and in epithelium, ACh causes secretion |
| What are the ENS neurons that contain inhibitory substances known as? | Noncholinergic, nonadrenergic inhibitory neurons (NANC neurons) |
| What is the advantage for some enteric reflexes to be transmitted to prevertebral ganglia? | ENS neurons synapse frequently, and bypassing these neurons by transmitting signals to prevertebral ganglia speeds up communication between segments of the gut. |
| Define ileus | A functional intestinal obstruction caused by an inhibition of motor activity due to mechanical obstruction, surgery, or peritonitis. |
| Describe the reflex activity associated with simple obstruction. | Initial inhibition of motor activity caudal to obstruction and increased activity cranially ("descending inhibition"). Persistence is followed by more inhibition, and then pain. |
| Instead of catecholamines, what substances released from postganglionic adrenergic and enteric nerves induce inhibition? | NPY and NO |
| Where are the enteroendocrine cells located and what do they synthesize? | EE cells are distributed throughout the gastric, intestinal, and pancreatic tissue. They synthesize peptide hormones and amines that are released upon stimulation. |
| How are the EE secretions transmitted? | True endocrine transmission via blood and paracrine transmission in the immediate vicinity of the cell |
| How does the location of the cells that secrete gastrin, CCK, and secretin correlate with their function? | Located in the stomach and proximal small intestine, and are responsible for initiation of gastric and intestinal phases of digestion |
| How does the location of cells secreting enteroglucagon and peptide YY correlate with their function? | Located in the distal small intestine, make up the "ileal brake" to slow gastric emptying and SI transit and increase SI absorption |
| Describe the influence of systemic hormones on enteric function. | Systemic hormones primarily affect extracellular fluid volume and arterial pressure. Epinephrine and aldosterone ^ Na and water absorption in intestine and colon. ANP increases Na and water secretion. Angiotensin ^absorption in SI. Epi & angio constrict. |
| What part of the intestinal wall is involved in the secretion of substances with paracrine effects? | Lamina propria |
| What is the role of basal amounts of paracrine substances and specifically prostaglandins and NO? | Physiological functions (protection and maintenance of mucosal epithelial barrier, mucosal blood flow, etc. |
| What four classes of growth factors are present in the GI tract? What cells secrete them? | Epidermal growth factor, transforming growth factor, insulin-like growth factor, and fibroblast growth factor. Secreted by epithelial and lamina proprial cells. |
| What are the roles of histamine and serotonin secreted by mast cells? | Have direct actions on smooth muscle cell contractility and epithelial cell electrolyte secretion. |
| What is the signaling function of the hydrogen peroxide secreted by phagocytes? | Stimulates epithelial cells to secrete ions and water, also stimulates fibroblasts to release prostaglandins, which also stimulate epithelial secretion. |
| Describe how prehension differs in the domestic species. | Dog/cat: head and jaws Horse: lips Cows/sheep: tongue and incisor teeth Pig: snout and lower lip Liquid is sucked by most species, but dogs and cats for a ladle with the tongue. |
| What is the difference in the innervation between striated and smooth muscle of the esophagus? | Smooth: myenteric plexus serves as a relay between vagal preganglionic fibers and muscle cells Striated: motor end plates and efferent fibers |
| What is the purpose of primary versus secondary peristalsis? | Primary: perstaltic contraction of the esophagus elicited only by a swallowing movement Secondary: stimulated by the presence of a bolus/foreign body |
| How does the slow wave set the "pace" for muscle contraction? | Slow waves set the maximal possible frequency of contractions because the depolarization wave must reach a critical threshold for spike action potentials to occur. |
| What two mechanisms induce increases in cytosolic calcium concentration? | 1) ACh binding, IP3 causes release of Ca 2) Opening of voltage gated calcium channels on plasma membrane |
| Describe the mechanical function of the three motor zones of the stomach. | Fundus: reception and storage of food (can relax to accomodate more) Corpus: mixing gastric juice and food Antrum: pump (pyloric sphincter, propulsion into duodenum or back into cardia) |
| How does the motor function of the antrum result int he separation of liquid and particles and how does this affect the rate of emptying? | Liquids pass through the pyloric sphincter and solids do not. Solids are forced back into the body for more grinding/mixing. Pyloric tone thus slows emptying. |
| What is the neural mechanism for increasing the rate of gastric emptying? | Rate at which fluid contents leave the stomach is regulated by receptors in the duodenum that respond to the chemical composition of a meal, volume, mechanoreceptors in the wall of the stomach. |
| What neural and hormonal mechanisms are responsible for decreasing the rate of gastric emptying and where are they located? | Governed primarily by CCK and sympathetic reflexes. CCK receptors monitor fat content. Sympathetic duodenal receptors monitor chemical composition. |
| What in the gastric contents triggers the neural and hormonal mechanisms that slow gastric emptying? | If digesta is hypertonic, acidic, irritating; too carby, fatty, or proteiny - sympathetic receptors slow emptying. |
| What are the consequences of uncontrolled gastric emptying? | Osmotic imbalance, duodenal ulceration, inability to absorb nutrients. |
| Why does the vomitus sometimes contain small intestinal contents? | Relaxation of the proximal intestine will sweep intestinal contents back into the stomach. |
| What neural centers are involved in the central and reflex control of vomiting? | Two centers in medulla: the vomiting center (reticular formation) and the chemoreceptor trigger zone (floor of fourth ventricle). |
| What nerves are involved in the central and reflex control of vomiting? | VC directly controlled by afferents in GI tract (vagal and sympathetic nn.). Efferent cranial motor nerves innervate upper GI and spinal nerves innervate diaphragm and abdominal mm. CTZ receives central stimulus from chemicals (apomorphine) >> VC |
| Why does vomiting sometimes result in metabolic alkalosis? | Loss of H ion in the vomitus |
| Describe how two muscle coats coordinate contractions that result in either segmental contractions or peristalsis. | Contraction of longitudinal mm. and inhibition of circular mm. distal to the bolus expand the lumen, while inhibition of longitudinal mm. and contraction of circular mm. proximal to the bolus propel it forward. 2nd intrinsic reflex is segmental, mixes. |
| Can these two patterns of contraction be controlled by local innervation or do they require mediation by the CNS? | Inhibitory reflexes (splanchnic intestino-intestine inhibitory reflex and vagal afferents from mechanoreceptors) and excitatory reflexes (vago-vagal reflex) |
| Describe how the digestive and intendigestive patterns of motility differ in regards to gastric emptying and intestinal transit. | Small intestinal motility usually segmental, with short distances traveled by peristalsis. Interdigestive period motility is called migrating myoelectric complex. |
| What are the three phases of the MMC and how do they differ in the percentage of slow waves that result in muscle contraction. | I: slow waves but no action potentials II: occasional action potentials III: bursts of spikes during slow waves, resulting in strong peristaltic contraxns and propulsion through stomach and SI. Pylorus relaxed, stomach emptied. |
| How do the digestive and interdigestive patterns differ in a carnivore and herbivore? How does this affect overall velocity of intestinal transit? | In carnivores and omnivores, a fed pattern occurs for six hours after feeding, while in ruminants and horses don't have a fed period. Due to compensatory mechanisms, transit times end up being almost equal. |
| How is the rapid velocity of intestinal transit associated with the uninterrupted MMC compensated for in the ruminant? | Long small intestine and constant outflow of contents from the reticulorumen |
| Describe the neural and/or hormonal controls that initiate the fed pattern of motility in the stomach and SI. | Stomach: initiated by hormones (gastrin) Intestine: extrinsic innervation (vago-vagal reflex due to nutrient density) |
| What types of motor activity are responsible for delaying transit in the LI and why is this important to colonic function? | Stationary haustral contractions mix ingesta and act as a barrier to flow. Propulsive movements go in aborial and oral directions and impede flow. |
| How does slow wave activity differ from that seen in the SI and where are the dominant pacemakers located? | In the LI slow waves move both orally and aborally. Pacemakers are located in the proximal and mid colon. |
| Describe the electrical activity associated with increased transit in intestinal parasitism. | Increased rate of emptying is associated with shorter duration of and decreased numbers of MMC, which are replaced by MAPC signals. |
| What resident immune cells are responsible for initiating the altered motility in parasitism or allergy? | Mast cells (have receptors for IgE) |
| How do mast cells communicate with nerves and what is the role of nerves in the altered motility? | Histamine and serotonin stimulate enteric nerves, which stimulate muscle and epithelium. |
| What are the major functions of saliva in the dog versus the ruminant? | In the dog, saliva is used in evaporative cooling and in mastication (contains amylase). In the ruminant, saliva is secreted in large amounts and is essential to microbial digestion (lubrication and buffering). |
| What is the cellular mechanism for forming the primary secretion? | Primary secretion involves Na and water. An Na-K-Cl pump on the basal membrane loads the cell with Cl, which then diffuses into the lumen. Na flows in and out of the cell to maintain neutrality. |
| Describe the mechanism for bicarb production and absorption. | Cells can be modified to excrete bicarb instead of Cl, through the apical anion conductance pathway. Reabsorption occurs when H ion is secreted into the saliva. |
| How does aldosterone affect transport in the duct system? | Aldosterone causes Na and water reabsorption in the duct system. |
| What mechanisms account for the major differences in salivary composition between ruminants and nonruminants? | In ruminants, upregulation of the Na/K/ATPase pump excretes excess dietary K and allows for water conservation. In nonruminants, water is not reabsorbed from the saliva due to low conductance in the epithelium, and therefore saliva can become hypotonic. |
| What products are secreted by the stomach? | Most important include H ion, pepsinogen, mucus, HCO3, intrinsic factor, and water. Also gastrin and somatostatin. |
| Describe the differences in the distribution of gastric mucosa in the dog versus the horse. | Dog: majority proper gastric tissue, cardiac and stratified sq. near esophagus and pyloric near pyloric sphincter Horse: majority strat. sq., followed by cardiac, some proper gastric, and pyloric |
| Name three substances that stimulate gastric acid secretion. Where do these substances originate? | ACh: cholinergic neurons Gastrin: G cells in the pyloric region Histamine: ECL cells or mast cells in mucosa |
| In which area of gastric mucosa are the parietal, chief, gastrin, and D cells found? | Parietal (HCl): proper gastric mucosa Chief (pepsinogen): proper gastric mucosa Gastrin: pyloric region D (somatostatin): pyloric region |
| What is the function of an enterochromaffin-like cell? | ECL cells release histamine in the proper gastric mucosa, which regulates acid-pepsin secretion (~paracrine cells). |
| What ion enters the blood for every H ion secreted into the gastric lumen? | Potassium via the H-K ATPase pump |
| What substances stimulate gastrin release and what primary mechanism inhibits gastrin release? | Proteins from feeding stimulate gastrin release, which stimulates ECL cells to release histamine which stimulates parietal cells to secrete HCl. Inhibition occurs via acidification of the stomach (somatostatin released, acts on endocrine cells). |
| Why is the stomach more acidic during the interdigestive period? | Stomach contents neutralize the gastric acid, stimulating gastrin release, which acidifies the stomach. As food leaves, pH drops further, inhibiting gastrin release and maintaining a low pH. |
| How does the gastric mucosal barrier differ in the stratified squamous versus the proper gastric mucosal zones? | Stratified: high electrical resistance, which restricts the movement of H ions Proper gastric: secretes mucus, which acts as a barrier and secretes bicarb |
| Discuss the pathophysiology of peptic ulcer disease in the stratified squamous mucosal zone of the pig stomach. How does this mechanism differ from peptic ulcer disease in the body or the antrum of the stomach? | Ulceration of the ss mucosa usually results from finely ground diets that cause higher fluidity of gastric contents and loss of stratification (high acid/pepsin region extends to ss mucosa which has less protection). |
| Which cells secrete sodium bicarbonate and which secrete enzymes? Where are they located in the pancreas? | Pancreatic centroacinar cells secrete bicarb, while the acinar cells secrete enzymes. Acinar cells are located in duct lumens, while centroacinar celss are located in the proxicmal ducts. |
| Why does the plasma become acidified during pancreatic bicarbonate secretion? | H ion is secreted into the blood by the Na-H exchanger in the basolateral membrane (energized by NaK ATPase) and HCO3 is lost due to the resulting rxn. |
| How does the regulation of the cystic fibrosis transmembrane conductance regulator control bicarb secretion? | Regulation of HCO3 secretion is acheived by regulating the CFTR Cl channel because transport of HCO3 across the membrane is coupled with transport of Cl into the cell. |
| Why is pancreatic bicarbonate secretion necessary? | Secretion of bicarb by the pancreas exactly neutralizes the HCl secreted by the stomach into the duodenum, maintaining acid/base balance both in the duodenum and the blood. |
| What intestinal hormones control pancreatic secretion and what stimluates their release? | CCK is released in the proximal intestine in response to amino and fatty acids in the lumen >enzymes. Secretin is released in response to acid, and stimulates release of NaHCO3. |
| How does "potentiation" occur in respect to the interaction of secretin and CCK? | Secretin can signal through cAMP, which up-regulates CFTR activity, which increases release of HCO3. CCK acts with Ca 2nd messenger system to increase enzyme release. |
| How does the flow of bile into the intestine differ in the horse and dog? | Horse: continuous (no gallbladder) Dog: sphincter of Oddi closed between meals, opened by CCK in response to fat |
| What is the difference between hepatic and gallbladder bile: | Hepatic: presence of water and electrolytes in addition to bile salts, lipids Gallbladder: water and electrolytes absorbed, bile salts more concentrated |
| In which direction does blood and bile flow in a liver lobule? | Blood: blood from hepatic artery and and portal vein flows into sinusoids to central vein Bile: drains peripherally into ductules and then ducts in portal triad |
| How do protein-bound molecules access the hepatocyte? | Sinusoidal endothelium has large pores, allowing protein into the extravascular fluid around hepatocytes |
| What form are the majority of bile salts in at the pH of the intestine? | Biles salts are conjugated at the pH of the intestine, making them insoluble and retaining them in the intestinal lumen. |
| In what part of the intestine are the majority of the bile salts reabsorbed? Why in only this segment? | Bile salts are reabsorbed in the ileum, after they've done their job in fat digestion but before they can do damage to colonic epithelial damage. |
| What anatomical mechanisms increase the small-intestine surface area? | Circumferential folds, villi, and microvilli |
| What are the general functional differences between the small and large intestine? | Small: microvillar digestion (surface), nutrient absorption except SCFA's Large: ability to conserve Na, SCFA absorption, no surface digestion |
| Define four cellular phenotypes on the small intestine epithelium. | 1) columnar absorptive cells 2) goblet cells 3) enterochromaffin cells (endocrine fx) 4) undifferentiated cells |
| Why does the tip of the villus receive blood with the lowest arterial PO2? | As blood flows into the central arteriole, oxygen diffuses down its concentration gradient into the veins draining the villus. |
| What is a possible consequence of nonocclusive intestinal ischemia on the mucosa of the small intestine? | Damaged mucosa allows toxic substances (ie endotoxin) to be absorbed from the lumen. |
| Why does reperfusion of a previously ischemic bowel sometimes lead to worsening of the villous damage? | ATP is catabolyzed into a molecule that reacts with oxygen to create oxygen radicals, which also recruit neutrophils (further damage) |
| What are the phases and sites of assimilation of carbohydrates, proteins, and fat? | Pancreatic phase: intestinal lumen Mucosal phase: brush border surface, cytoplasm Delivery phase: portal vein |
| Name the three end products of carbohydrate digestion that are absorbed in the portal blood? | Glucose, fructose, and galactose |
| What is the function of bile in the jejunum? | Micelle formation` |
| By what process are fatty acids absorbed across the brush border? | Chylomicrons (protein coat allows transport out of cell) and micelles (allows transport into cell) |
| Why is absorption of intact protein important in the neonate? | to allow direct absorption of immunoglobulins. |
| What are the carbohydrate sources and absorbable end products of microbial digestion of carbohydrate? | Sources: starch and fiber Digested to hexoses, and turned into SCFA's and gas |
| What are the primary differences in utilization of microbial protein between ruminants and horses? | Ruminants are able to utilize microbial protein, while hindgut fermenters (horses) cannot. |
| Most of the salt and water that the gut has to reabsorb is derived from what sources? | Endogenous sources |
| Why is the magnitude of the enterosystemic circulation much greater in herbivores than in carnivores? | Herbivores require massive amounts of salivation due to their fermentative digestion |
| What forces govern bulk water flow across the epithelium and into the capillary bed? | Osmotic and hydrostatic gradients set up by the basolateral membrane Na-K pumps. |
| What two cellular transport mechanisms are responsible for sodium absorption by the small-intestine epithelium? | Neutral NaCl absorptive processes and Na-coupled cotransport processes |
| What is the site and what is the basic driving force for intestinal secretion of salt and water? | Na-K ATPase pump on the basolateral membrane |
| How do the mechanisms for Ca absorption differ than those for other electrolytes? | Does not use the Na gradient mechanism. Kept at an extremely low intracellular concentration and enters via facillitated diffusion. |
| How doe the SCFA's become undissociated (lipid soluble) in the large intestine lumen? | H2CO3 sheds an H ion, which protonates the SCFA anion and causes it to be lipid soluble. |
| Name some paracrine mediators that promote intestinal secretion. | Serotonin, prostaglandins, ACh, histamine |
| What class of systemic hormones mediates intestinal absorption? | The renin-angiotensin-aldosterone system: activated by a decrease in ECFV sensed by baroreceptors in renal vessels; angio II promotes absorption in the jejunum via norepi and ileal absorption via neutral NaCl processes and in colon via aldosterone |
| How do the mechanisms producing diarrhea in rotovirus infection differ from that produced during e. coli infection? | E. coli produces enterotoxins, which cause intestinal hypersecretion, whereas rotavirus causes villous atrophy resulting in maldigestion/malabsorption. |
| Describe the mechanisms by which intestinal inflammation induces intestinal secretion and malabsorption. | Enterotoxins attach to apical membrane receptors, increasing cAMP and cGMP, which inhibit NaCl absorption and induce anion secretion from the crypts, leading to massive hypersecretion. |
| What is epithelial "restitution"? | The immediate response of the mucosa to injury and loss of epithelium. Viable cells below the injury travel (ameboid) to the defect and spread to cover the injury. |
| How does proliferation differ from restitution? | It occurs very quickly, is an intrinsic motion process caused by signaling from the basement membrane. |
| By what means are the polyamine levels raised in the crypt cells? | Reaction mediated by ornithine decarboxylase, which is stimulated by gastrin/GF's. Also from diet, shedding of mature cells, secretion. |
| Why does villous contraction assist the repair process in a damaged epithelium? | Villous contraction reduces height, allowing the entire surface to be covered. |
| How many stomach compartments do true ruminants have? | Four: nonsecretory rumen, reticulum, and omasum, and a secretory abomasum |
| What is the principal digestive role of the forestomach? | Microbial fermentation of ingesta, usually through hydrolysis and anaerobic oxidation. SCFA's used as primary metabolic substrates. |
| How is the surface area of the lining membrane increased in the stomach compartments? | Characteristic folding: rumen is studded by papillae and reticulum looks like honeycomb. |
| Based on fiber number ratios, which activity of vagal and splanchnic innervation predominates, motor or sensory? | Majority sensory nerves |
| How do the motor activities of the vagal and splanchnic nerves differ? | Vagal: parasympathetic, major contraction cycles Splanchnic: sympathetic, when stimulated inhibit mobility |
| How do the functions of tension receptors and epithelial/mucosal receptors differ? | Tension: slowly adapting mechanoreceptors located in series with contractile elements Epithelial: rapidly adapting mechanoreceptors and chemoreceptors |
| In what ways to pseudoruminants and the true ruminants differ? | Pseudoruminants have a two-compartment forestomach, and lack a true omasum. They also have primitive dentition. |
| What are the benefits and the costs of the ruminant type of digestion? | Benefits: utilization of fibrous diets, ability to break down cellulose and fiber, sythesis of microbial protein from many sources, synthesis of B vitamins Costs: constant eating, lots of chewing, complicated mechanisms to keep rumen healthy |
| What are the optimal conditions for the fermentative environment? | Regular addition of new food, presence of suitable numbers and types of microbes, removal of end products, mixing, propulsion of unfermented material, anaerobic environment, and stable conditions |
| What are the main types of ruminal microbe? | Bacteria, yeast-like fungi, and protozoa |
| What are the main fermentative processes? | Hydrolysis and anaerobic oxidation |
| What are the functional groupings of the ruminal bacteria? | Primary: digest actual dietary components Secondary: use end products of primary |
| What are the main activities of the protozoa? | Feed on ruminal bacteria and other readily digestible materials: used as a source of microbial protein in lean times, prevent overproliferation of bacteria |
| What is meant by the stratification of ruminal contents? | Layer of gas on top of raft of fibrous material, which floats on the underlying layer of "soupy" fluid |
| What are the substrates and end products of each of the three stages of fermentation? | 1: Hydrolysis of plant polysaccharides to monosaccharides and then to fructose 2: anaerobic oxidation of fructose 1,6-bisphosphate to pyruvate 3: Pyruvate to CH4, CO2, acetate, butyrate, and propionate |
| In what ways does the fermentation of cellulose and starch differ? | Cellulose: done slowly by primary celluloytic bacteria, all 4 stages Starch: done quickly by primary amylolytic bacteria, not always 4 stages |
| What are the origins of nitrogenous compounds in the rumen? | Diet, NPN's, endogenous urea; most are transformed by extracellular proteases and absorbed, processed into amino acids or ammonia |
| What VFA's are produced by fermentation? | acetic, proprionic, and butyric acids from carbs; valeric acid and branched VFA's from proteins |
| What mechanisms normally prevent a fall in rumen pH despite the continuous production of VFA's? | Carbonic anhydrase in epithelium produces bicarb and H ion, which associates with VFA's and neutralizes them. |
| How is each of the principal VFA's utilized? | Butyric acid: metabolized to ketone body (beta hydroxy butyrate) Proprionate: converted to oxaloacetate and lactic acid, which are used in gluconeogenesis Acetate: prime metabolic substrate, used to make acetyl coA |
| What causes lactic acid to accumulate when there is an abrupt switch to starch-rich diets? | Amylolytic bacteria |
| What are the consequences of lactic acid accumulation? | metabolic acidosis |
| What is the rate of gas production in cattle following a meal? | 40L per hour for 2 to 4 hours after a meal |
| What are the origins and fates of the gases of fermentation? | CO2: decarboxylation reactions of fermentation and neutralization of H ion CH4: reduction of CO2 and formate by methanogenic bacteria H2S: reduction from sulfates and from sulfur containing a.a.'s H2: abnormal fermentation O2: diffusion and eating |
| How does mastication affect salivation? | Movements of teeth excite the sensory buccal mechanoreceptors around the teeth sockets, which stimulate the most potent excitatory inputs to the salivary glands and gastric centers. |
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